TCF7L2 lncRNA: a link between bipolar disorder and body mass index through glucocorticoid signaling

Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI), which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription...

Celý popis

Uloženo v:

Podrobná bibliografie
Vydáno v:	Molecular psychiatry Ročník 26; číslo 12; s. 7454 - 7464
Hlavní autoři:	Liu, Duan, Nguyen, Thanh Thanh Le, Gao, Huanyao, Huang, Huaizhi, Kim, Daniel C, Sharp, Brenna, Ye, Zhenqing, Lee, Jeong-Heon, Coombes, Brandon J, Ordog, Tamas, Wang, Liewei, Biernacka, Joanna M, Frye, Mark A, Weinshilboum, Richard M
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England Nature Publishing Group 01.12.2021
Témata:	Astrocytes Bipolar disorder Bipolar Disorder - genetics Body Mass Index Central nervous system Chromatin Diabetes mellitus Diabetes Mellitus, Type 2 - metabolism Gene polymorphism Genes Genome-wide association studies Genome-Wide Association Study Genomes Glucocorticoids Humans Immunoprecipitation Induced Pluripotent Stem Cells - metabolism Insulin Non-coding RNA Pancreas Pluripotency Polymorphism, Single Nucleotide - genetics Quantitative trait loci RNA, Long Noncoding - genetics Single-nucleotide polymorphism Stem cells Transcription Factor 7-Like 2 Protein - genetics Transcription Factor 7-Like 2 Protein - metabolism
ISSN:	1359-4184, 1476-5578, 1476-5578
On-line přístup:	Získat plný text
Tagy:	Přidat tag Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!

Abstract	Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI), which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in the BD and BMI interaction remained unclear. In the present study, we demonstrated by studying human induced pluripotent stem cell (hiPSC)-derived astrocytes, cells that highly express TCF7L2 in the CNS, that the BD-BMI GWAS risk SNP is associated with glucocorticoid-dependent repression of the expression of a previously uncharacterized TCF7L2 transcript variant. That transcript is a long non-coding RNA (lncRNA-TCF7L2) that is highly expressed in the CNS but not in peripheral tissues such as the liver and pancreas that are involved in metabolism. In astrocytes, knockdown of the lncRNA-TCF7L2 resulted in decreased expression of the parent gene, TCF7L2, as well as alterations in the expression of a series of genes involved in insulin signaling and diabetes. We also studied the function of TCF7L2 in hiPSC-derived astrocytes by integrating RNA sequencing data after TCF7L2 knockdown with TCF7L2 chromatin-immunoprecipitation sequencing (ChIP-seq) data. Those studies showed that TCF7L2 directly regulated a series of BD risk genes. In summary, these results support the existence of a CNS-based mechanism underlying BD-BMI genetic risk, a mechanism based on a glucocorticoid-dependent expression quantitative trait locus that regulates the expression of a novel TCF7L2 non-coding transcript.
AbstractList	Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI), which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in the BD and BMI interaction remained unclear. In the present study, we demonstrated by studying human induced pluripotent stem cell (hiPSC)-derived astrocytes, cells that highly express TCF7L2 in the CNS, that the BD-BMI GWAS risk SNP is associated with glucocorticoid-dependent repression of the expression of a previously uncharacterized TCF7L2 transcript variant. That transcript is a long non-coding RNA (lncRNA-TCF7L2) that is highly expressed in the CNS but not in peripheral tissues such as the liver and pancreas that are involved in metabolism. In astrocytes, knockdown of the lncRNA-TCF7L2 resulted in decreased expression of the parent gene, TCF7L2, as well as alterations in the expression of a series of genes involved in insulin signaling and diabetes. We also studied the function of TCF7L2 in hiPSC-derived astrocytes by integrating RNA sequencing data after TCF7L2 knockdown with TCF7L2 chromatin-immunoprecipitation sequencing (ChIP-seq) data. Those studies showed that TCF7L2 directly regulated a series of BD risk genes. In summary, these results support the existence of a CNS-based mechanism underlying BD-BMI genetic risk, a mechanism based on a glucocorticoid-dependent expression quantitative trait locus that regulates the expression of a novel TCF7L2 non-coding transcript.Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI), which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in the BD and BMI interaction remained unclear. In the present study, we demonstrated by studying human induced pluripotent stem cell (hiPSC)-derived astrocytes, cells that highly express TCF7L2 in the CNS, that the BD-BMI GWAS risk SNP is associated with glucocorticoid-dependent repression of the expression of a previously uncharacterized TCF7L2 transcript variant. That transcript is a long non-coding RNA (lncRNA-TCF7L2) that is highly expressed in the CNS but not in peripheral tissues such as the liver and pancreas that are involved in metabolism. In astrocytes, knockdown of the lncRNA-TCF7L2 resulted in decreased expression of the parent gene, TCF7L2, as well as alterations in the expression of a series of genes involved in insulin signaling and diabetes. We also studied the function of TCF7L2 in hiPSC-derived astrocytes by integrating RNA sequencing data after TCF7L2 knockdown with TCF7L2 chromatin-immunoprecipitation sequencing (ChIP-seq) data. Those studies showed that TCF7L2 directly regulated a series of BD risk genes. In summary, these results support the existence of a CNS-based mechanism underlying BD-BMI genetic risk, a mechanism based on a glucocorticoid-dependent expression quantitative trait locus that regulates the expression of a novel TCF7L2 non-coding transcript. Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI), which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in the BD and BMI interaction remained unclear. In the present study, we demonstrated by studying human induced pluripotent stem cell (hiPSC)-derived astrocytes, cells that highly express TCF7L2 in the CNS, that the BD-BMI GWAS risk SNP is associated with glucocorticoid-dependent repression of the expression of a previously uncharacterized TCF7L2 transcript variant. That transcript is a long non-coding RNA (lncRNA-TCF7L2) that is highly expressed in the CNS but not in peripheral tissues such as the liver and pancreas that are involved in metabolism. In astrocytes, knockdown of the lncRNA-TCF7L2 resulted in decreased expression of the parent gene, TCF7L2, as well as alterations in the expression of a series of genes involved in insulin signaling and diabetes. We also studied the function of TCF7L2 in hiPSC-derived astrocytes by integrating RNA sequencing data after TCF7L2 knockdown with TCF7L2 chromatin-immunoprecipitation sequencing (ChIP-seq) data. Those studies showed that TCF7L2 directly regulated a series of BD risk genes. In summary, these results support the existence of a CNS-based mechanism underlying BD-BMI genetic risk, a mechanism based on a glucocorticoid-dependent expression quantitative trait locus that regulates the expression of a novel TCF7L2 non-coding transcript.
Author	Kim, Daniel C Lee, Jeong-Heon Coombes, Brandon J Weinshilboum, Richard M Sharp, Brenna Wang, Liewei Ye, Zhenqing Liu, Duan Frye, Mark A Biernacka, Joanna M Huang, Huaizhi Gao, Huanyao Ordog, Tamas Nguyen, Thanh Thanh Le
Author_xml	– sequence: 1 givenname: Duan orcidid: 0000-0003-1065-246X surname: Liu fullname: Liu, Duan organization: Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA – sequence: 2 givenname: Thanh Thanh Le orcidid: 0000-0002-2281-6540 surname: Nguyen fullname: Nguyen, Thanh Thanh Le organization: Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN, USA – sequence: 3 givenname: Huanyao orcidid: 0000-0002-9441-9579 surname: Gao fullname: Gao, Huanyao organization: Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA – sequence: 4 givenname: Huaizhi surname: Huang fullname: Huang, Huaizhi organization: Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN, USA – sequence: 5 givenname: Daniel C orcidid: 0000-0003-0919-3569 surname: Kim fullname: Kim, Daniel C organization: Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA – sequence: 6 givenname: Brenna surname: Sharp fullname: Sharp, Brenna organization: Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA – sequence: 7 givenname: Zhenqing surname: Ye fullname: Ye, Zhenqing organization: Division of Computational Biology, Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA – sequence: 8 givenname: Jeong-Heon surname: Lee fullname: Lee, Jeong-Heon organization: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA – sequence: 9 givenname: Brandon J orcidid: 0000-0003-4322-5923 surname: Coombes fullname: Coombes, Brandon J organization: Division of Computational Biology, Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA – sequence: 10 givenname: Tamas orcidid: 0000-0002-3940-7284 surname: Ordog fullname: Ordog, Tamas organization: Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA – sequence: 11 givenname: Liewei orcidid: 0000-0003-3818-8531 surname: Wang fullname: Wang, Liewei organization: Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA – sequence: 12 givenname: Joanna M orcidid: 0000-0001-9350-4440 surname: Biernacka fullname: Biernacka, Joanna M organization: Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA – sequence: 13 givenname: Mark A orcidid: 0000-0001-6997-4215 surname: Frye fullname: Frye, Mark A email: MFrye@mayo.edu organization: Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA. MFrye@mayo.edu – sequence: 14 givenname: Richard M orcidid: 0000-0002-4911-7985 surname: Weinshilboum fullname: Weinshilboum, Richard M email: Weinshilboum.Richard@mayo.edu organization: Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA. Weinshilboum.Richard@mayo.edu
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/34535768$$D View this record in MEDLINE/PubMed
BookMark	eNpd0E1LAzEQBuAgFfuhf8CDBLx4Wc13st5KsSoUBannJbvJtqnbpCa7aP31rlgvnmZgHl5mZgwGPngLwDlG1xhRdZMYpgpliOAMYSJZ9nUERphJkXEu1aDvKc8zhhUbgnFKG4R-hvwEDCnjlEuhRqBazuZyQWDjq5en6S3UsHH-DZa2_bDWw9LtQqMjNC6FaGyE2htYBrOHW50SdN7YT9iuY-hWa7hquipUIbauCs7A5FZe92mrU3Bc6ybZs0OdgNf53XL2kC2e7x9n00VWCSTbjNQ2J5RTS4SVjGJFDVE5LXFZq7K_QmJbE5prZBQxFAkp85rlgkrGNMalphNw9Zu7i-G9s6ktti5Vtmm0t6FLBeE9RZwJ1NPLf3QTutiv2ytBCVNECtGri4Pqyq01xS66rY774u999Bt6hXIE
CitedBy_id	crossref_primary_10_1186_s13058_024_01861_2 crossref_primary_10_1038_s42003_025_08563_1 crossref_primary_10_1093_nar_gkac1045 crossref_primary_10_3389_fcell_2022_1046357 crossref_primary_10_1158_1078_0432_CCR_20_4774 crossref_primary_10_3390_genes14010213 crossref_primary_10_1016_j_jpsychires_2022_09_032 crossref_primary_10_3390_ijms252212404 crossref_primary_10_1016_j_jpsychires_2024_01_007 crossref_primary_10_1038_s41380_023_02281_y crossref_primary_10_1176_appi_ajp_20230921 crossref_primary_10_1016_j_gene_2024_148670 crossref_primary_10_1161_CIRCRESAHA_123_323200 crossref_primary_10_1016_j_jgg_2024_01_001
ContentType	Journal Article
Copyright	2021. The Author(s). The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml	– notice: 2021. The Author(s). – notice: The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID	CGR CUY CVF ECM EIF NPM 3V. 7TK 7X7 7XB 88E 88G 8AO 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FYUFA GHDGH GNUQQ HCIFZ K9. LK8 M0S M1P M2M M7P PHGZM PHGZT PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS PSYQQ Q9U 7X8
DOI	10.1038/s41380-021-01274-z
DatabaseName	Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Neurosciences Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Psychology Database (Alumni) ProQuest Pharma Collection ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central Natural Science Collection ProQuest One ProQuest Central Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Biological Sciences ProQuest Health & Medical Collection Medical Database Psychology Database Biological Science Database ProQuest One Academic ProQuest One Academic (New) ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic (retired) ProQuest One Academic UKI Edition ProQuest Central China ProQuest One Psychology ProQuest Central Basic MEDLINE - Academic
DatabaseTitle	MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) ProQuest One Psychology ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Biological Science Collection ProQuest Central Basic ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest Psychology Journals (Alumni) Biological Science Database ProQuest SciTech Collection Neurosciences Abstracts ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest Psychology Journals ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic
DatabaseTitleList	MEDLINE - Academic ProQuest One Psychology MEDLINE
Database_xml	– sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Biology
EISSN	1476-5578
EndPage	7464
ExternalDocumentID	34535768
Genre	Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural
GrantInformation_xml	– fundername: NIDDK NIH HHS grantid: R01 DK126827 – fundername: NIAAA NIH HHS grantid: R01 AA027486 – fundername: NIGMS NIH HHS grantid: U19 GM061388 – fundername: NIDDK NIH HHS grantid: R01 DK058185 – fundername: NIGMS NIH HHS grantid: R01 GM028157
GroupedDBID	--- -Q- 0R~ 123 29M 2WC 36B 39C 4.4 406 53G 70F 7X7 88E 8AO 8FI 8FJ 8R4 8R5 AACDK AANZL AASML AATNV AAYZH ABAKF ABAWZ ABBRH ABDBE ABDBF ABFSG ABIVO ABJNI ABLJU ABRTQ ABUWG ABZZP ACAOD ACGFS ACKTT ACPRK ACRQY ACSTC ACUHS ACZOJ ADBBV AEFQL AEJRE AEMSY AENEX AEVLU AEXYK AEZWR AFBBN AFDZB AFHIU AFKRA AFRAH AFSHS AGAYW AGHAI AGQEE AHMBA AHSBF AHWEU AIGIU AILAN AIXLP AJRNO ALFFA ALIPV ALMA_UNASSIGNED_HOLDINGS AMYLF ATHPR AXYYD AYFIA AZQEC B0M BAWUL BBNVY BENPR BHPHI BKKNO BPHCQ BVXVI CAG CCPQU CGR COF CS3 CUY CVF DIK DNIVK DPUIP DU5 DWQXO E3Z EAD EAP EBC EBD EBLON EBS ECM EE. EIF EIOEI EJD EMB EMK EMOBN EPL EPS ESX F5P FDQFY FEDTE FERAY FIGPU FIZPM FSGXE FYUFA GNUQQ HCIFZ HMCUK HVGLF HZ~ IAO IHR INH INR IPY ITC IWAJR JSO JZLTJ KQ8 M1P M2M M7P NPM NQJWS O9- OK1 OVD P2P PHGZM PHGZT PJZUB PPXIY PQGLB PQQKQ PROAC PSQYO PSYQQ Q2X RNS RNT RNTTT ROL SNX SNYQT SOHCF SOJ SRMVM SV3 SWTZT TAOOD TBHMF TDRGL TEORI TR2 TSG TUS UKHRP ~8M 3V. 7TK 7XB 8FE 8FH 8FK K9. LK8 PKEHL PQEST PQUKI PRINS Q9U 7X8 PUEGO
ID	FETCH-LOGICAL-c607t-2fe92353e26e743183d2893b1bf8b41871ef239a0d82d306779f4963744a11ba3
IEDL.DBID	M7P
ISICitedReferencesCount	19
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000696811900001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	1359-4184 1476-5578
IngestDate	Fri Sep 05 08:54:20 EDT 2025 Tue Oct 07 05:14:23 EDT 2025 Mon Jul 21 05:59:24 EDT 2025
IsDoiOpenAccess	false
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	12
Language	English
License	2021. The Author(s).
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c607t-2fe92353e26e743183d2893b1bf8b41871ef239a0d82d306779f4963744a11ba3
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
ORCID	0000-0002-2281-6540 0000-0003-4322-5923 0000-0002-3940-7284 0000-0003-1065-246X 0000-0003-0919-3569 0000-0002-4911-7985 0000-0002-9441-9579 0000-0001-6997-4215 0000-0001-9350-4440 0000-0003-3818-8531
OpenAccessLink	https://pubmed.ncbi.nlm.nih.gov/PMC8872993
PMID	34535768
PQID	2632482766
PQPubID	44096
PageCount	11
ParticipantIDs	proquest_miscellaneous_2574405460 proquest_journals_2632482766 pubmed_primary_34535768
PublicationCentury	2000
PublicationDate	2021-12-01
PublicationDateYYYYMMDD	2021-12-01
PublicationDate_xml	– month: 12 year: 2021 text: 2021-12-01 day: 01
PublicationDecade	2020
PublicationPlace	England
PublicationPlace_xml	– name: England – name: New York
PublicationTitle	Molecular psychiatry
PublicationTitleAlternate	Mol Psychiatry
PublicationYear	2021
Publisher	Nature Publishing Group
Publisher_xml	– name: Nature Publishing Group
SSID	ssj0014765
Score	2.4712613
Snippet	Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of...
SourceID	proquest pubmed
SourceType	Aggregation Database Index Database
StartPage	7454
SubjectTerms	Astrocytes Bipolar disorder Bipolar Disorder - genetics Body Mass Index Central nervous system Chromatin Diabetes mellitus Diabetes Mellitus, Type 2 - metabolism Gene polymorphism Genes Genome-wide association studies Genome-Wide Association Study Genomes Glucocorticoids Humans Immunoprecipitation Induced Pluripotent Stem Cells - metabolism Insulin Non-coding RNA Pancreas Pluripotency Polymorphism, Single Nucleotide - genetics Quantitative trait loci RNA, Long Noncoding - genetics Single-nucleotide polymorphism Stem cells Transcription Factor 7-Like 2 Protein - genetics Transcription Factor 7-Like 2 Protein - metabolism
Title	TCF7L2 lncRNA: a link between bipolar disorder and body mass index through glucocorticoid signaling
URI	https://www.ncbi.nlm.nih.gov/pubmed/34535768 https://www.proquest.com/docview/2632482766 https://www.proquest.com/docview/2574405460
Volume	26
WOSCitedRecordID	wos000696811900001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LaxsxEB6apIVc-n64TY0KvYrs6u1eShpieqgXE1LwzegJhnTXjZ1A-uurkZX01F56EbvssitGo9GM5tN8AB8jzz6_dJ7mpZ3RfC3ohLWKihSMY5J76VMhm9BdZxaLybxuuG0qrPLOJhZDHQaPe-THpa64YVqpz-ufFFmjMLtaKTT24ACrJLAC3ZvfZxGELlSSLZeY7TSiHpppuDneZONtGooABUy-Cvrr7y5mWWqmT_63k0_hcXUyyclOK57Bg9g_h0c72snbF-AvTqf6GyOXvT_vTj4RSzCNSypki7jVGuNdEmphTmL7QNwQbsmP7GmTUl-RVH4fUiDvOYLNfxpWgSAcxOIJ95fwfXp2cfqVVrIF6lWjt5SlmH09ySNTEb0Kw0OOxbhrXTIuC0-3MTE-sU0wLGCcoSdJ5NmrhbBt6yx_Bfv90Mc3QISPnFluVWisSKmxSanGOGOtdCxENYKjO-kt64zZLP-IbgQf7h9nXccEhu3jcJ3fkVjOUArVjOD1boSW611RjiUXkmPs9PbfH38HhwwHvQBSjmB_e3Ud38NDf7Ndba7GsKcXurRmDAdfzrr5eb6bsdm4KFZuu_nsN2of0TM
linkProvider	ProQuest
linkToHtml	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Lb9NAEB6VAoILzwJpCywSHFe19-VNJVRVhahV0wihIPVm9ilFAjs0KSj8KH4jO2unnODWAzdLttay5_POjOeb-QBeB55ifmkdTa6d0XQs6JCViorotWWSO-liFpuoJhN9fj78sAG_1r0wSKtc74l5o_atw3_ke3muuGaVUgfzbxRVo7C6upbQ6GBxGlY_Usq2eHvyLtn3DWOj99OjY9qrClCnimpJWQwpqJE8MBXQfWruU9LBbWmjtqJMCUSIjA9N4TXzGFBXwygSTCshTFlaw9O6N-CmwJZRpAqys6uqhaiydGXJJVZXteibdAqu9xbJWeiCIiECi72C_vx7SJtd2-j-__ZSHsC9Pogmhx3qH8JGaB7B7U5Wc_UY3PRoVI0Z-dK4j5PDfWIIlqlJT0kjdjbHfJ74fvAoMY0ntvUr8jVlEiTPjyS9fhHJlP6Uoac7tTNPkO5isIN_Cz5dyxM-gc2mbcIzIMIFzgw3yhdGxFiYqFShrTZGWuaDGsDu2lp1vyMs6j-mGsCrq9PpW8YCjWlCe5mukTiuUQpVDOBph4h63g0dqbmQHHPD7X8v_hLuHE_PxvX4ZHK6A3cZAi6Tb3Zhc3lxGZ7DLfd9OVtcvMjQJfD5umHxG8ikJTk
linkToPdf	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1da9RAFL3UrRZf_K5urTqCPg6bzFdmCyK17WJpCUup0Lc4n7CgydrdKutP89d5J8nWJ33rg2-BhAnJnMy9J_fMPQBvAsecX1pHMbQziseCjlmuqIheWya5ky62ZhNFWeqLi_F0A36t98IkWeV6TWwXat-49I981PYV16xQahR7WcT0cPJ-_o0mB6lUaV3baXQQOQmrH0jfFu-OD3Gu3zI2OTo_-Eh7hwHqVFYsKYsBExzJA1MhhVLNPRIQbnMbtRU5kokQGR-bzGvmU3JdjKNAyBZCmDy3huO4t2CzwCRDDGDzw1E5PbuuYYiiNbLMuUy1Vi36LTsZ16MFhg6d0SSPSKVfQX_-PcFtA93k_v_8ih7AvT69Jvvd9_AQNkL9CO50hpurx-DODybFKSNfandW7u8RQ1IBm_RiNWJn88T0ie9bkhJTe2IbvyJfkWOQtrMk6Z2NSCv2R-6Od2pmniQhjEl7-5_Apxt5wm0Y1E0dngERLnBmuFE-MyLGzESlMm21MdIyH9QQdtczV_VrxaL6M21DeH19Gr_yVLoxdWiu8BqZGjlKobIhPO3QUc27diQVF5In1rjz78FfwRaioTo9Lk-ew12WsNeqcnZhsLy8Ci_gtvu-nC0uX_Y4JvD5pnHxG78hL1M
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=TCF7L2+lncRNA%3A+a+link+between+bipolar+disorder+and+body+mass+index+through+glucocorticoid+signaling&rft.jtitle=Molecular+psychiatry&rft.au=Liu%2C+Duan&rft.au=Nguyen+Thanh+Thanh+Le&rft.au=Gao+Huanyao&rft.au=Huang+Huaizhi&rft.date=2021-12-01&rft.pub=Nature+Publishing+Group&rft.issn=1359-4184&rft.eissn=1476-5578&rft.volume=26&rft.issue=12&rft.spage=7454&rft.epage=7464&rft_id=info:doi/10.1038%2Fs41380-021-01274-z&rft.externalDBID=HAS_PDF_LINK
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1359-4184&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1359-4184&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1359-4184&client=summon